Pyoderma gangrenosum
Pyoderma gangrenosum jẹ toje, arun ara iredodo nibiti awọn pustules irora tabi awọn nodules di ọgbẹ ti o dagba ni ilọsiwaju. Pyoderma gangrenosum kii ṣe akoran. Awọn itọju le pẹlu awọn corticosteroids, ciclosporin, tabi orisirisi awọn egboogi monoclonal. Bi o tilẹ jẹ pe o le ni ipa lori awọn eniyan ti ọjọ ori eyikeyi, o ṣe pataki julọ awọn eniyan ti o wa ni 40s ati 50s.
☆ Ninu awọn abajade 2022 Stiftung Warentest lati Jẹmánì, itẹlọrun alabara pẹlu ModelDerm jẹ kekere diẹ ju pẹlu awọn ijumọsọrọ telemedicine isanwo.
Lori ese eniyan ti o ni ulcerative colitis.
References
Pyoderma gangrenosum jẹ ipo awọ ti o ṣọwọn ti o fa awọn ọgbẹ irora pẹlu awọn eti pupa tabi purplish. O ti pin si bi arun iredodo ati pe o jẹ apakan ti ẹgbẹ kan ti a pe ni awọn dermatoses neutrophilic. Idi ti pyoderma gangrenosum jẹ idiju, pẹlu awọn iṣoro pẹlu ajẹsara innate ati adaṣe ni awọn eniyan ti o ni itara jiini. Laipe, awọn oniwadi ti dojukọ lori follicule irun bi aaye ibẹrẹ ti o pọju ti arun na.
Pyoderma gangrenosum is a rare inflammatory skin disease classified within the group of neutrophilic dermatoses and clinically characterized by painful, rapidly evolving cutaneous ulcers with undermined, irregular, erythematous-violaceous edges. Pyoderma gangrenosum pathogenesis is complex and involves a profound dysregulation of components of both innate and adaptive immunity in genetically predisposed individuals, with the follicular unit increasingly recognized as the putative initial target.
Pyoderma gangrenosum is a rare inflammatory skin disease classified within the group of neutrophilic dermatoses and clinically characterized by painful, rapidly evolving cutaneous ulcers with undermined, irregular, erythematous-violaceous edges. Pyoderma gangrenosum pathogenesis is complex and involves a profound dysregulation of components of both innate and adaptive immunity in genetically predisposed individuals, with the follicular unit increasingly recognized as the putative initial target.
Pyoderma gangrenosum jẹ ipo awọ to ṣọwọn ti o fa awọn adaijina irora pupọ. Lakoko ti a ko loye idi rẹ ni kikun, a mọ pe o kan iṣẹ ṣiṣe ti o pọ si ti awọn sẹẹli ajẹsara kan. Atọju arun na ko tun rọrun. A ni awọn oogun oriṣiriṣi ti o dinku eto ajẹsara tabi ṣe atunṣe iṣẹ ṣiṣe rẹ. Lẹgbẹẹ awọn wọnyi, a tun ni idojukọ lori atọju awọn ọgbẹ ati iṣakoso irora. Awọn Corticosteroids ati cyclosporine nigbagbogbo jẹ yiyan akọkọ fun itọju, ṣugbọn laipẹ, iwadii diẹ sii ti wa lori lilo awọn itọju biologic bi awọn inhibitors TNF-α. Awọn onimọ-jinlẹ wọnyi jẹ ayanfẹ pupọ sii, paapaa ni awọn alaisan ti o ni awọn ipo iredodo miiran, ati pe wọn nlo ni iṣaaju ninu ilana arun na.
Pyoderma gangrenosum is a rare neutrophilic dermatosis that leads to exceedingly painful ulcerations of the skin. Although the exact pathogenesis is not yet fully understood, various auto-inflammatory phenomena with increased neutrophil granulocyte activity have been demonstrated. Despite the limited understanding of the pathogenesis, it is no longer a diagnosis of exclusion, as it can now be made on the basis of validated scoring systems. However, therapy remains a major multidisciplinary challenge. Various immunosuppressive and immunomodulatory therapies are available for the treatment of affected patients. In addition, concomitant topical pharmacologic therapy, wound management and pain control should always be addressed. Corticosteroids and/or cyclosporine remain the systemic therapeutics of choice for most patients. However, in recent years, there has been an increasing number of studies on the positive effects of biologic therapies such as inhibitors of tumour necrosis factor-α; interleukin-1, interleukin-17, interleukin-23 or complement factor C5a. Biologics have now become the drug of choice in certain scenarios, particularly in patients with underlying inflammatory comorbidities, and are increasingly used at an early stage in the disease rather than in therapy refractory patients.
Pyoderma gangrenosum is a rare neutrophilic dermatosis that leads to exceedingly painful ulcerations of the skin. Although the exact pathogenesis is not yet fully understood, various auto-inflammatory phenomena with increased neutrophil granulocyte activity have been demonstrated. Despite the limited understanding of the pathogenesis, it is no longer a diagnosis of exclusion, as it can now be made on the basis of validated scoring systems. However, therapy remains a major multidisciplinary challenge. Various immunosuppressive and immunomodulatory therapies are available for the treatment of affected patients. In addition, concomitant topical pharmacologic therapy, wound management and pain control should always be addressed. Corticosteroids and/or cyclosporine remain the systemic therapeutics of choice for most patients. However, in recent years, there has been an increasing number of studies on the positive effects of biologic therapies such as inhibitors of tumour necrosis factor-α; interleukin-1, interleukin-17, interleukin-23 or complement factor C5a. Biologics have now become the drug of choice in certain scenarios, particularly in patients with underlying inflammatory comorbidities, and are increasingly used at an early stage in the disease rather than in therapy refractory patients.
